Trypanosoma brucei brucei infects a wide range of mammals but is unable to infect humans because this T. brucei subspecies is lyzed by NHS1,2. In contrast, Trypanosoma brucei rhodesiense exhibits sensitivity or resistance to normal human serum (NHS), depending on antigenic variation. The latter phenotype arises because the gene encoding resistance, serum resistance associated protein (SRA), is present in a single of the multiple polycistronic units where the genes for the variant antigen, the variant surface glycoprotein (VSG), can be transcribed4. The product of serum resistance associated protein (SRA) is an atypical variant surface glycoprotein (VSG), shorter than average (410 aa instead of approximately 490)3. Anti-SRA antibodies detected a protein around 50 kDa (FIG. 1 lanes 1,2), which accumulates in the lysosome as revealed with specific markers for the endocytic compartment, namely tomato lectin (flagellar pocket, endosomes and lysosome)5 and antibodies against the lysosomal membrane glycoprotein p676 (FIG. 2a,b).